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    段中鑫, 覃玉蓉, 夏新莉, 尹伟伦. 超量表达胡杨peuMIR156j基因增强拟南芥耐盐性[J]. 北京林业大学学报, 2011, 33(6): 1-7.
    引用本文: 段中鑫, 覃玉蓉, 夏新莉, 尹伟伦. 超量表达胡杨peuMIR156j基因增强拟南芥耐盐性[J]. 北京林业大学学报, 2011, 33(6): 1-7.
    DUAN Zhong-xin, QIN Yu-rong, XIA Xin-li, YIN Wei-lun. Overexpression of Populus euphratica peuMIR156j gene enhancing salt tolerance in Arabidopsis thaliana[J]. Journal of Beijing Forestry University, 2011, 33(6): 1-7.
    Citation: DUAN Zhong-xin, QIN Yu-rong, XIA Xin-li, YIN Wei-lun. Overexpression of Populus euphratica peuMIR156j gene enhancing salt tolerance in Arabidopsis thaliana[J]. Journal of Beijing Forestry University, 2011, 33(6): 1-7.

    超量表达胡杨peuMIR156j基因增强拟南芥耐盐性

    Overexpression of Populus euphratica peuMIR156j gene enhancing salt tolerance in Arabidopsis thaliana

    • 摘要: MicroRNAs (miRNAs)是一类内源性的非编码小分子RNA。本文克隆了miR156j的前体(peuMIR156j),并将其转入拟南芥获得35S:MIR156j转基因植株。对转基因植株的鉴定表明,过量表达miR156j增加了拟南芥莲座叶的发生,导致叶片浓密及开花延迟。这一结果表明:同拟南芥、水稻等物种类似,胡杨miR156j主要对植株发育起重要作用,其功能具有保守性。同时发现超表达胡杨miR156j的拟南芥在盐处理下萌发率与生长状况优于野生型,RTPCR检测显示靶基因SPL6、SPL9及SPL11的表达下调,证明它们被miR156j负调控。基于预测的与逆境胁迫相关的靶基因STRS2(逆境响应抑制物2),推断出miR156j可能通过调控STRS2而发挥耐盐功能的分子机制。

       

      Abstract: MicroRNAs (miRNAs) is a class of endogenous non-coding small molecule RNA. To analyze the biological function of Populus euphratica miR156j, miR156j precursor(peuMIR156j)was cloned and transferred into Arabidopsis thaliana, and 35S:MIR156j transgenic plants were obtained in the current work. The results showed that overexpression of miR156j increased the number of rosette leaves, leading to thick leaves and delayed flowering, which was similar to A. thaliana,rice, etc. P. euphratica miR156j conservatively played a main role in plant development. Also germination rate and growth condition of 35S:MIR156j transgenic A. thaliana under salt treatment were better than that of the wild type, and the expression assay of gene SPL6, SPL9 and SPL11 demonstrated the downregulation caused by miR156 Based on the predicted stressassociated target gene STRS2(stress response suppressor 2), we presumed that the molecular mechanism underlying the involvement of miR156 in salttolerance may be ascribed to the regulation of STRS2 expression.

       

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